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Background: This study delves into the complex interplay among prostate-specific antigen, alkaline phosphatase, and the temporal dynamics of tumor shrinkage in prostate cancer. By investigating the longitudinal trajectories and time-to-prostate cancer tumor shrinkage, we aim to untangle the intricate patterns of these biomarkers. This understanding is pivotal for gaining profound insights into the multifaceted aspects of prostate cancer progression. The joint model approach serves as a comprehensive framework, facilitating the elucidation of intricate interactions among these pivotal elements within the context of prostate cancer .
Methods: A new joint model under a shared parameters strategy is proposed for mixed bivariate longitudinal biomarkers and event time data, for obtaining accurate estimates in the presence of missing covariate data. The primary innovation of our model resides in its effective management of covariates with missing observations. Built upon established frameworks, our joint model extends its capabilities by integrating mixed longitudinal responses and accounting for missingness in covariates, thus confronting this particular challenge. We posit that these enhancements bolster the model's utility and dependability in real-world contexts characterized by prevalent missing data. The main objective of this research is to provide a model-based approach to get full information from prostate cancer data collected with patients' baseline characteristics ( , body mass index ( ), , , and ) and two longitudinal endogenous covariates ( and ).
Results: The results reveal a clear association between prostate-specific antigen and alkaline phosphatase biomarkers in the context of time-to-prostate cancer tumor shrinkage. This underscores the interconnected dynamics of these key indicators in gauging disease progression.
Conclusions: The analysis of the prostate cancer dataset, incorporating a joint evaluation of mixed longitudinal prostate-specific antigen and alkaline phosphatase biomarkers alongside tumor status, has provided valuable insights into disease progression. The results demonstrate the effectiveness of the proposed joint model, as evidenced by accurate estimates. The shared variables associated with both longitudinal biomarkers and event times consistently deviate from zero, highlighting the robustness and reliability of the model in capturing the complex dynamics of prostate cancer progression. This approach holds promise for enhancing our understanding and predictive capabilities in the clinical assessment of prostate cancer.
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http://dx.doi.org/10.1186/s12894-024-01522-8 | DOI Listing |
JAMA Netw Open
September 2025
Department of Urology, Center for Health Outcomes Research and Dissemination, University of Washington, Seattle.
Importance: Black individuals have a twofold higher rate of prostate cancer death in the US compared with the average population with prostate cancer. Few guidelines support race-conscious screening practices among at-risk Black individuals.
Objective: To examine structural factors that facilitate or impede access to prostate cancer screening among Black individuals in the US.
J Oncol Pharm Pract
September 2025
Department of Research & Development, Squad Medicine and Research (SMR), Amadalavalasa, Andhra Pradesh, India.
Cancer vaccines represent a transformative shift in oncology, aiming to prevent malignancies or treat established cancers by training the immune system to recognize tumor-specific or tumor-associated antigens. This review explores the diverse platforms and mechanisms supporting cancer vaccines, ranging from prophylactic vaccines such as HPV and hepatitis B vaccines that have significantly reduced virus-related cancers to therapeutic vaccines like Sipuleucel-T and T-VEC that extend survival in prostate cancer and melanoma. Vaccine types are classified, and delivery platforms including mRNA, peptide, dendritic cell and viral vector-based approaches are examined alongside pivotal clinical trial outcomes.
View Article and Find Full Text PDFEndocr Relat Cancer
September 2025
Department of Molecular, Cell and Developmental Biology, University of California Los Angeles;Los Angeles, CA 90095.
Age is a major risk factor for a range of diseases including prostate cancer. Understanding how age influences the susceptibility of normal prostate epithelial cells to cancer initiation is complicated by the fact that aging affects all tissues in the body. Assessing how various aging mechanisms influence the prostate epithelium is a necessary step to determine the critical factors associated with aging that increase prostate cancer risk.
View Article and Find Full Text PDFEndocr Connect
September 2025
Dysfunction of several WD40 family proteins causes diverse endocrine diseases. Until recently, MEP50, a WD40 protein, was considered a Gene of Unknown Significance (GUS) because no inherited diseases had been linked to its function. However, genetic inactivation of MEP50 in mouse models or somatic mutations in humans drive oncogenesis in several endocrine-related cancers, including those of the prostate, breast, and uterus.
View Article and Find Full Text PDFFront Genet
August 2025
Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Background: Prostatic diseases, consisting of prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa), pose significant health challenges. While single-omics studies have provided valuable insights into the role of mitochondrial dysfunction in prostatic diseases, integrating multi-omics approaches is essential for uncovering disease mechanisms and identifying therapeutic targets.
Methods: A genome-wide meta-analysis was conducted for prostatic diseases using the genome-wide association studies (GWAS) data from FinnGen and UK Biobank.